title: Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease.
abstract: OBJECTIVE
  We sought to examine whether patients with stable coronary artery disease (CAD) have increased platelet reactivity and an enhanced propensity to form monocyte-platelet aggregates.
  
  
  BACKGROUND
  Platelet-dependent thrombosis and leukocyte infiltration into the vessel wall are characteristic cellular events seen in atherosclerosis.
  
  
  METHODS
  Anticoagulated peripheral venous blood from 19 patients with stable CAD and 19 normal control subjects was incubated with or without various platelet agonists and analyzed by whole blood flow cytometry.
  
  
  RESULTS
  Circulating degranulated platelets were increased in patients with CAD compared with control subjects (mean [+/- SEM] percent P-selectin-positive platelets: 2.1 +/- 0.2 vs. 1.5 +/- 0.2, p < 0.01) and were more reactive to stimulation with 1 micromol/liter of adenosine diphosphate (ADP) (28.7 +/- 3.9 vs. 16.1 +/- 2.2, p < 0.01), 1 micromol/liter of ADP/epinephrine (51.4 +/- 4.6 vs. 37.5 +/- 3.8, p < 0.05) or 5 micromol/liter of thrombin receptor agonist peptide (TRAP) (65.7 +/- 6.8 vs. 20.2 +/- 5.1, p < 0.01). Patients with stable CAD also had increased circulating monocyte-platelet aggregates compared with control subjects (percent platelet-positive monocytes: 15.3 +/- 3.0 vs. 6.3 +/- 0.9, p < 0.01). Furthermore, patients with stable CAD formed more monocyte-platelet aggregates than did control subjects when their whole blood was stimulated with 1 micromol/liter of ADP (50.4 +/- 4.5 vs. 28.1 +/- 5.3, p < 0.01), 1 micromol/liter of ADP/epinephrine (60.7 +/- 4.3 vs. 48.0 +/- 4.8, p < 0.05) or 5 micromol/liter of TRAP (67.6 +/- 5.7 vs. 34.3 +/- 7.0, p < 0.01).
  
  
  CONCLUSIONS
  Patients with stable CAD have circulating activated platelets, circulating monocyte-platelet aggregates, increased platelet reactivity and an increased propensity to form monocyte-platelet aggregates.
authors.affiliation: Cardiovascular Thrombosis Research Center, Department of Medicine, University of Massachusetts Medical Center, Worcester 01655, USA. mark.furman@banyan.ummed.edu
authors.forename: M I
authors.initials: MI
authors.lastname: Furman
authors.forename: S E
authors.initials: SE
authors.lastname: Benoit
authors.forename: M R
authors.initials: MR
authors.lastname: Barnard
authors.forename: C R
authors.initials: CR
authors.lastname: Valeri
authors.forename: M L
authors.initials: ML
authors.lastname: Borbone
authors.forename: R C
authors.initials: RC
authors.lastname: Becker
authors.forename: H B
authors.initials: HB
authors.lastname: Hechtman
authors.forename: A D
authors.initials: AD
authors.lastname: Michelson
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D000787:Angina Pectoris / Q000097:blood / Q000473:pathology; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000494:pharmacology; D002452:Cell Count; D015550:Cell Degranulation; D002465:Cell Movement; D003324:Coronary Artery Disease / Q000473:pathology; D003327:Coronary Disease / Q000097:blood* / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007962:Leukocytes / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000502:physiology*; D019007:P-Selectin / Q000032:analysis; D010446:Peptide Fragments / Q000494:pharmacology; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology*; D018179:Receptors, Thrombin / Q000819:agonists; D013927:Thrombosis / Q000097:blood
chemical_list: D015815:Cell Adhesion Molecules; D019007:P-Selectin; D010446:Peptide Fragments; D018179:Receptors, Thrombin; C072032:thrombin receptor peptide (42-55); D000244:Adenosine Diphosphate; D004837:Epinephrine